Case Report Cheating the CHA DS -VASc Score...

Case ReportCheating the CHA2DS2-VASc Score: Thromboembolism inApical Hypertrophic Cardiomyopathy

Robin A. P. Weir,1 Nicola MacKenzie,1 and Colin J. Petrie2

1 Cardiology Department, Hairmyres Hospital, East Kilbride, Glasgow G75 8RG, Scotland2 Cardiology Department, Monklands Hospital, Airdrie, Scotland

Correspondence should be addressed to Robin A. P. Weir; [email protected]

Received 23 September 2014; Revised 11 November 2014; Accepted 12 November 2014; Published 20 November 2014

Academic Editor: Yoko Miyasaka

Copyright © 2014 Robin A. P. Weir et al. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properlycited.

Atrial fibrillation increases the risk of systemic thromboembolism in general and stroke in particular. Not all patients whodevelop atrial fibrillation are at significantly heightened risk of thromboembolic complications, however, with the developmentof risk scoring systems aiding clinicians in determining whether formal anticoagulation is mandated. The most commonly usedcontemporary scoring systems—CHADS

2and CHA

2DS2-VASc—provide a reliable means of assessing stroke risk, but certain

cardiac conditions are associated with an increased incidence of thromboembolism without impacting on these risk scores.Hypertrophic cardiomyopathy, with its apical variant, is such a condition. We present a case of a patient with apical hypertrophiccardiomyopathy and atrial fibrillation who suffered dire thromboembolic consequences despite a reassuringly low CHA

2DS2-VASc

score and suggest that this scoring system ismodified to incorporate the thromboembolic risk inherent to certain cardiomyopathiesirrespective of impairment of left ventricular systolic dysfunction or clinical heart failure.

1. Introduction

Contemporary scoring systems such as CHADS2

andCHA2DS2-VASc assist in prediction of the risk of systemic

thromboembolism in patients with paroxysmal or persis-tent/permanent atrial fibrillation (AF) but fail to acknowl-edge the risk associated with certain cardiomyopathies lead-ing to inappropriate undertreatment of at-risk patients.

2. Case Presentation

A 45-year-old male nonsmoker presented with a 2-hourhistory of acute pain in his left foot. His family doctor haddetected 4 weeks previously at a routine annual health checkthat he was in AF and had arranged an echocardiogramwhich had shown marked hypertrophy of the apical leftventricular (LV) cavity (Figure 1(a), arrows), with obliterationof the midcavity in systole (Figure 1(b), arrows), appearancesconsistent with apical hypertrophic cardiomyopathy (HCM).

There was no evidence of apical aneurysm formation, LV sys-tolic function was within normal limits (LV ejection fraction(LVEF) calculated at 59% using Simpson’s biplane method),and there were no valvular abnormalities.There was no othersignificant previous medical history, and anticoagulation hadnot been recommended due to his calculated CHA

2DS2-

VASc score of 0 [1].Physical examination on admission revealed a healthy but

distressed patient with a pulse of 80 beats per minute irreg-ularly irregular, blood pressure 150/57mmHg, and absentleft lower limb pulses distal to the left femoral pulse. Theleft foot was pale and cold with capillary refill delayed at5 seconds, although no signs of cutaneous necrosis werepresent. Vascular examination of the right lower limb wasnormal. There were no added heart sounds or murmursand no signs of cardiac decompensation. A 12-lead electro-cardiogram was recorded, which confirmed AF (ventricularrate 72 beats per minute) with widespread deep T-waveinversion (Figure 2).Within 4 hours of admission to hospital,the patient underwent uncomplicated surgical left femoral

Hindawi Publishing CorporationCase Reports in CardiologyVolume 2014, Article ID 189895, 3 pageshttp://dx.doi.org/10.1155/2014/189895

2 Case Reports in Cardiology

LV

(a) (b)

Figure 1: Apical hypertrophic cardiomyopathy. Transthoracic echocardiogram showing left ventricular (LV) apical hypertrophy in diastole((a), arrows) and midcavity obliteration at end-systole ((b), arrows).

Figure 2: Preoperative ECG. Atrial fibrillation with voltage criteriafor left ventricular hypertrophy and deep inferior/anterolateral T-wave inversion.

embolectomy which restored adequate left lower limb perfu-sion.The patient was anticoagulated with warfarin and madean uncomplicated recovery, completing 24 weeks of warfarintherapy prior to cessation of formal anticoagulation (largelyat the request of the patient, who had had recurrent epistaxiswhile on warfarin). Unfortunately, he suffered a disablingstroke 10 weeks after stopping warfarin, with evidence of aright temporoparietal infarct on CT brain imaging. Dopplerultrasonography of the carotid arteries was normal, with theclinical impression that he had suffered a further cardioem-bolic event. Warfarin was reinstituted and recommended aslifelong therapy following the acute phase of the stroke.

3. Discussion

The fact that the risk of systemic embolism in patients withnonvalvular AF is higher in older age and in the presenceof hypertension, diabetes, or a prior cerebrovascular eventis well documented [2]. Warfarin reduces the incidenceof stroke in high-risk patients with nonvalvular AF butdetermining which patients merit lifelong anticoagulationremains challenging [3]. The CHADS

2score—incorporating

congestive heart failure (CHF), hypertension, age ≥ 75,diabetes, and prior stroke/transient ischemic attack (TIA)—has been superseded by the recent CHA

2DS2-VASc score [1].

This latter score assigns a point each for CHF, hypertension,diabetes, prior vascular event, female sex, and age ≥ 65, with

double points awarded for age ≥ 75 and/or a prior stroke/TIA.Annualized stroke rates range from 0% for CHA

2DS2-VASc 0

to 15.2% for a score of 9 (the highest possible) [1].Whilst a CHA

2DS2-VASC score of 0 does not equate to

zero risk of thromboembolism, the risk of ischaemic strokein males with AF and a CHA

2DS2-VASc score of 0 is not

significantly higher than age and sex-matched controls insinus rhythm [4]. Anticoagulation is usually recommendedfor CHA

2DS2-VASc ≥1, which equates to a stroke risk of

1.3% per annum. Despite a diagnosis of apical HCM, thesubject of this study had a CHA

2DS2-VASC score of 0 at

the outset, having never had clinical heart failure and withpreserved LV systolic function.The apical variant is reportedin up to ∼7% of Western and ∼25% of Asian patients withHCM [4, 5]. Long-term outcome studies have shown thatapical HCM is not associated with increased cardiovascularmortality but heart failure, arrhythmias (particularly AF),and myocardial infarction are more common [6]. Studiesof patients with AF and HCM (incorporating apical HCM)have reported a stroke rate of 3.75% per 100 patients perannum [7]. The mechanism by which apical HCM increasesthe risk of thromboembolism is unclear. Apical segmentaldysfunctionwith consequent aneurysm formation, which hasbeen observed to occur in the absence of epicardial coronaryartery disease and is perhaps related to microvascular diseaseand reduced coronary flow reserve, is a potential mechanism,compounded by local eddying and stagnation of blood flow[8]. Left atrial enlargement is an independent risk factor forstroke in patients with AF; the management of the patientwith HCM (apical or other) and left atrial enlargement butwithout documented atrial arrhythmia remains challeng-ing, although at present prophylactic anticoagulation is notwarranted. We recommend rigorous monitoring for atrialarrhythmias in such patients.

Failure to score a point on the CHA2DS2-VASc score

at the time of diagnosis of this patient with AF and HCMreassured the attending physician that the risk of systemicembolism was sufficiently low to negate the requirementfor formal anticoagulation. We caution physicians attending

Case Reports in Cardiology 3

patients with AF and a cardiomyopathy without impair-ment of systolic function to determine the risk of systemicembolism for the individual patient and suggest that the cur-rent definition of the “C” inCHA

2DS2-VASc—heart failure or

moderate-to-severe LV systolic dysfunction (LVEF ≤ 40%)—should perhaps be modified with an acknowledgement ofthe risk that certain cardiomyopathies impose despite theabsence of heart failure or significant systolic dysfunction [1].

Conflict of Interests

The authors declare that there is no conflict of interestsregarding the publication of this paper.

References

[1] G. Y. H. Lip, R. Nieuwlaat, R. Pisters, D. A. Lane, and H. J.G. M. Crijns, “Refining clinical risk stratification for predictingstroke and thromboembolism in atrial fibrillation using a novelrisk factor-based approach: the Euro Heart Survey on atrialfibrillation,” Chest, vol. 137, no. 2, pp. 263–272, 2010.

[2] “Risk factors for stroke and efficacy of antithrombotic therapy inatrial fibrillation: analysis of pooled data from five randomizedcontrolled trials,” Archives of Internal Medicine, vol. 154, no. 13,pp. 1449–1457, 1994.

[3] “Warfarin versus aspirin for prevention of thromboembolism inatrial fibrillation: stroke prevention in atrial fibrillation II study,”The Lancet, vol. 343, pp. 687–691, 1994.

[4] T.-F. Chao, C.-J. Liu, S.-J. Chen et al., “Atrial fibrillation and therisk of ischemic stroke: does it still matter in patients with aCHA2DS2-VASc score of 0 or 1?” Stroke, vol. 43, no. 10, pp. 2551–

2555, 2012.[5] T. Chikamori, Y. L. Doi, M. Akizawa, Y. Yonezawa, T. Ozawa,

and W. J. McKenna, “Comparison of clinical, morphologi-cal, and prognostic features in hypertrophic cardiomyopathybetween Japanese and Western patients,” Clinical Cardiology,vol. 15, no. 11, pp. 833–837, 1992.

[6] C. R. Cannan, G. S. Reeder, K. R. Bailey, L. J. Melton III, andB. J. Gersh, “Natural history of hypertrophic cardiomyopathy:a population-based study, 1976 through 1990,” Circulation, vol.92, no. 9, pp. 2488–2495, 1995.

[7] M. J. Eriksson, B. Sonnenberg, A. Woo et al., “Long-termoutcome in patients with apical hypertrophic cardiomyopathy,”Journal of the American College of Cardiology, vol. 39, no. 4, pp.638–645, 2002.

[8] M. E. Bertrand, P. Y. Tilmant, J. M. Lablanche, and F. A.Thieuleux, “Apical hypertrophic cardiomyopathy: clinical andmetabolic studies,” European Heart Journal, vol. 4, pp. 127–133,1983.

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